Anatomical and Physiological Differences between

Review published: 14 December 2017 doi: 10.3389/fneur.2017.00685

Anatomical and Physiological Differences between Children and Adults Relevant to Traumatic Brain Injury and the Implications for Clinical Assessment and Care Anthony A. Figaji* Neuroscience Institute, Division of Neurosurgery, University of Cape Town, Red Cross Children’s Hospital, Rondebosch, Cape Town, South Africa

Edited by: Eric Peter Thelin, University of Cambridge, United Kingdom Reviewed by: Harish G. Vyas, University of Nottingham, United Kingdom Jason Luck, Duke University, United States *Correspondence: Anthony A. Figaji [email protected] Specialty section: This article was submitted to Neurotrauma, a section of the journal Frontiers in Neurology Received: 27 June 2017 Accepted: 30 November 2017 Published: 14 December 2017 Citation: Figaji AA (2017) Anatomical and Physiological Differences between Children and Adults Relevant to Traumatic Brain Injury and the Implications for Clinical Assessment and Care. Front. Neurol. 8:685. doi: 10.3389/fneur.2017.00685

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General and central nervous system anatomy and physiology in children is different to that of adults and this is relevant to traumatic brain injury (TBI) and spinal cord injury. The controversies and uncertainties in adult neurotrauma are magnified by these differences, the lack of normative data for children, the scarcity of pediatric studies, and inappropriate generalization from adult studies. Cerebral metabolism develops rapidly in the early years, driven by cortical development, synaptogenesis, and rapid myelination, followed by equally dramatic changes in baseline and stimulated cerebral blood flow. Therefore, adult values for cerebral hemodynamics do not apply to children, and children cannot be easily approached as a homogenous group, especially given the marked changes between birth and age 8. Their cranial and spinal anatomy undergoes many changes, from the presence and disappearance of the fontanels, the presence and closure of cranial sutures, the thickness and pliability of the cranium, anatomy of the vertebra, and the maturity of the cervical ligaments and muscles. Moreover, their systemic anatomy changes over time. The head is relatively large in young children, the airway is easily compromised, the chest is poorly protected, the abdominal organs are large. Physiology changes—blood volume is small by comparison, hypothermia develops easily, intracranial pressure (ICP) is lower, and blood pressure normograms are considerably different at different ages, with potentially important implications for cerebral perfusion pressure (CPP) thresholds. Mechanisms and pathologies also differ— diffuse injuries are common in accidental injury, and growing fractures, non-accidental injury and spinal cord injury without radiographic abnormality are unique to the pediatric population. Despite these clear differences and the vulnerability of children, the amount of pediatric-specific data in TBI is surprisingly weak. There are no robust guidelines for even basics aspects of care in children, such as ICP and CPP management. This is particularly alarming given that TBI is a leading cause of death in children. To address this, there is an urgent need for pediatric-specific clinical research. If this goal is to be achieved, any clinician or researcher interested in pediatric neurotrauma must be familiar with its unique pathophysiological characteristics. Keywords: children, traumatic brain injury, neurotrauma, brain, head

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WHY CHILDREN AND ADULTS ARE DIFFERENT

the cervical region; in younger patients, these are more often subluxations or dislocations, more often in the upper cervical spine, and more often associated with neurological injury (1–9). The fulcrum of movement descends from the upper cervical spine in young children, where C0–C2 injuries predominate, to progressively lower in the subaxial spine as they grow, when mid- to low cervical injuries become more common. The craniocervical junction is most vulnerable to injury and instability in young children because the articulations are more susceptible to movement than in older children, the ligaments and paraspinal muscles are weaker, and the dentocentral synchondrosis between the odontoid and C2 body are yet to fuse (5, 10). Congenital abnormalities of the dens and the atlas also increase susceptibility to injury. Careful attention must be paid to the lowermost axial images of the initial head computed tomography (CT), and the radiographer must ensure that craniocervical junction is well imaged: ligamentous injuries are common between C0 and C2 and are often manifest by retroclival hematomas (11, 12) (Figure 1). In pediatric spinal injury, four patterns tend to predominate: fracture with subluxation, fracture without subluxation, subluxation without fracture [purely ligamentous injury and spinal cord injury without radiographic abnormality (SCIWORA)] (5). SCIWORA is peculiar to children and is of particular concern

Adult physicians often underestimate the differences between adults and children. Those who work with children seldom do. Although children are very different from adults in physiology and disease, we commonly extrapolate data from adult traumatic brain injury (TBI) studies to pediatrics. At best this is often inappropriate; at worst it may be dangerous. The problem is that there are fewer studies in children, and so less evidence on which to base recommendations. Children are seen as a vulnerable population in ethics terms and so extrapolation from adult data is encouraged, which contributes to this practice. Its unintended consequence is weakened evidence to direct treatment for this most vulnerable population. This may be defendable if children were easier to treat than adults but unfortunately the converse is true. All of the difficulties and controversies of adult TBI are compounded in children. There are many examples. In children, the debate about thresholds for intracranial pressure (ICP) treatment are aggravated by the fact that normative values for ICP in children are not well established and depend on age. The same is true for blood pressure (BP), and so uncertainty about optimal cerebral perfusion pressure (CPP) thresholds is even greater. Resting and activated metabolic rates change across the childhood age range before settling into a reasonably stable pattern in adulthood, as does cerebral blood flow (CBF) and its response to injury. Clinical assessment is challenging—there are differences in the expected patterns of injury, clinical evaluation, imaging, and outcome assessment. Differences abound also in surgery: children have smaller blood volumes, reduced tolerance for blood loss, increased risks of long anesthesia, different reactions to medications, and reduced tissue perfusion—these are all challenging in children and so require special knowledge of TBI in childhood to optimize management. And that is not even mentioning the considerable anatomical differences. There can be little debate that children are indeed very different.

OVERVIEW Anatomy and physiology in children develops over several years to gradually assume the adult form. We need to be aware of these differences to prepare for common problems in childhood TBI.

CRANIAL AND SPINAL ANATOMICAL DIFFERENCES AND IMPLICATIONS FOR TREATMENT Relative to the size of a child’s body, the head is large and heavy, balanced on a neck poorly supported by weak muscles and ligaments, and so both head and cervical spine are easily injured. Biomechanical maturation of the spine is a progressive process that only starts to resemble the adult spine after age 8–9 years old. Epiphyses fuse at different times and are easily mistaken for fractures. The pattern of injuries is determined by these progressive changes. Most spine injuries in children occur in


Figure 1 | (A,C) Axial head computed tomography (CT) scan with low posterior fossa cuts revealing the retroclival hematomas anterior to the lower brainstem (arrowed); (B) CT surview showing atlanto-axial dislocation (arrowed); (D) sagittal T1 magnetic resonance imaging (MRI) showing retroclival hematoma (arrowed) better demonstrated on the subsequent MRI (13) (modified).

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because, by definition, radiographs are normal (14, 15). It reflects the easy deformation of the cervical spine with external loading and the risk to underlying neural structures. Several factors cause the cervical spine in children to be weaker and thus more easily deform: weaker cervical ligaments and paraspinal muscles, increased water content of intervertebral disks, unfused epiphyses, shallow facet joints, anteriorly wedged vertebral bodies, and undeveloped uncinate processes (16–23)—these all contribute to a more malleable spine that puts neural structures at risk, even without bony injury evident on radiographs. A high index of suspicion must be maintained, and magnetic resonance imaging (MRI) should promptly be done to investigate any signs of retroclival blood or long tract findings unexplained by the head injury (Figure 1). In awake patients, five clinical criteria have a high negative predictive value for significant spinal injury: normal alertness, absence of midline cervical tenderness, no focal deficit, no intoxication, and no painful distracting injury (9). The head and the brain are fundamentally different to adults physiologically and anatomically. In the newborn and infant, the head is disproportionally large and gradually assumes the head:body ratio of an adult over several years. Growth is particularly rapid in the first few years of life. At birth the brain is about 25% of the adult size even though body weight is about 5%; about half of the postnatal growth of the brain occurs in the first year or two; the ratio of head and neck length to body length (about 25%) in infants is almost double that of adults, and this is a continuum from gestational changes (24, 25). The disproportionally greater weight of the head also affects the movement of the head when a child falls or is struck by a moving object (26). The skull also undergoes considerable changes with age. Fontanels and sutures close at different times. At 2 months of age, the posterior fontanel is usually closed, and by 12–18 months, the anterior fontanel is closed. Open sutures and fontanels allow some buffering of ICP, especially if intracranial volume increases slowly, but only to some extent. In trauma, intracranial volume can increase rapidly, and so the increased compliance may be rapidly exhausted. Also, normal ICP in the very young is considerably lower than in adults, as is BP, so small increases in ICP may have significant adverse effects. The calvarium is thin in young children; this, with the sutures and fontanels, allows for easy deformation, with or without fracturing, under external pressure (27–30). Diastatic skull fractures may also occur in children (31), where an unfused suture diastases as a result of direct trauma or deformation, and sometimes with raised ICP. Because of the pliability of the skull, a linear fracture may represent significant underlying parenchymal injury sustained by marked deformation at the time of injury despite little evidence on the head CT. This makes growing skull fractures a unique feature of young children (32–35). At the moment of impact, the deformed bone and fractured edges tear the dura. Soft tissue interposes between the fractured edges which then do not heal. The pulsatility of the brain and the growth of the cranium then combine to increase the fracture size over time, which further retracts the dural edges in a vicious cycle. So, surveillance for growing fractures is important and these require surgery. On the other hand, closed depressed, “ping-pong,” fractures are common in very young children and


can often be treated conservatively. They often mold to normality over a few months. The thin skull may be a challenge for ICP monitoring—often surgeons are reluctant to use bolt systems or even measure ICP in the very young (36). If bolt systems are used in young children, the skull thickness must be measured on the head CT and the bolt thread adapted accordingly. Alternatively, the monitor can be tunneled. The young age of a patient should not be a reason not to monitor ICP. If the dura is intact, small skull defects often heal well due to the osteogenic potential in childhood bone; however, resorption rates after bone flap replacement are higher in young children (37), especially when there is a significant delay in the bone being replaced. The growing head size and pulsatile nature of the brain contribute not only to this risk but also to the problems of cranioplasty using foreign material (37, 38). Split calvarial grafts are ideal in this situation but unfortunately the underdeveloped medullary layer makes this difficult in children under the age of 3. Basal skull fractures are common, especially in crush injuries, in which release fractures may occur diagonally across the skull base. These must raise suspicion of an injury to the carotid artery (39) in the canal, especially when running into the sphenoid bone, and may warrant MR angiography. The vessel may be occluded by dissection and/or thrombus and this may be clinically silent in children if the crossflow through the circle of Willis is adequate. Even if the occlusion is asymptomatic, it is important to diagnose this because of the potential for thrombus extension. At the mild end of the spectrum, decision-making about head CT in children is compounded by the greater sensitivity of the developing brain to the effects of radiation, in terms of both cancer-inducing potential and cognitive development. Therefore, several sets of decision rules have been evaluated to rationalize the indications for head CT to limit over-investigation (40). Even if resources were not a problem, the solution is not as straightforward as lowering the threshold for MRI. Children under the age of 8 years old usually need sedation or general anesthesia for MRI, which carries relatively low risk, but risk nevertheless. Also, there is growing concern of the effects of long and cumulative anesthetics on the developing brain, although this remains controversial (41). The radiological pattern of pediatric TBI shows some differences to that of adult TBI (42). In severe pediatric TBI, diffuse injuries are more common than the focal injuries and contusions of adult TBI. In diffuse injuries, the scan looks relatively benign but the patient is in deep coma. A contusion in the midbrain is not uncommon as a manifestation of significant injury that may be subtle on head CT; MRI demonstrates the lesion more clearly. Patterns of injury are also determined by the mechanical properties of the brain tissue, which in children is stiffer than in adults (30). Non-accidental injury (“shaken baby syndrome”) is peculiar to young children (43, 44) and is beyond the scope of this article but is an important specific pathophysiological entity to be aware of. The pathophysiology, radiology, clinical presentation, and outcome are very different to accidental injury in many ways, and this requires separate consideration. Discrete hematomas in children are less common than in adults but of course do occur. Epidural hematomas in children 3


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are somewhat different to those in adults (45–47). The middle meningeal artery is not as incorporated into bone as in adults, but epidural bleeds from the edges of a fracture easily lead to hematomas. They occur in a wider variety of locations (Figure 2), in part because these are often due to venous rather than arterial hemorrhages (13). Fractures in the occipital and suboccipital regions are particularly concerning because of the risk of a posterior fossa hematoma, which rapidly causes brainstem compression as well as hydrocephalus by fourth ventricular and aqueduct obstruction (48–50). Subdural hematomas (Figure 3) are associated with more severe injuries to the parenchyma, cortical veins, and venous sinuses (51–53). Associated arterial and venous infarcts are not uncommon. Non-accidental injury must also be considered in infants where there are bilateral subdural collections, particularly of differing ages (28, 54); however, one must also keep in mind that there are other medical and procedure-related causes of subdural hematoma (53, 55–58).

are at particularly high risk of airway obstruction. Their tongues are relatively large for their oral cavity, as are the soft palate and soft tissues of the mouth and the epiglottis, which is relatively longer and stiff. They also have a larynx that is higher and more anterior, a cricoid ring that represents the narrowest point of the airway, and a shorter trachea that bifurcates higher (59, 60). The trachea has a small diameter and is compressible, so even small changes in diameter or foreign bodies can rapidly lead to airway compromise; frank respiratory embarrassment is accelerated by their reduced functional residual capacity and higher metabolic requirements per weight (61). Because they have a large occiput, their necks flex easily when lying supine, which may contribute to airway compromise. The chest wall is cartilaginous and more easily deformable; rib fractures are unusual but lung contusions are common and may be severe despite little external evidence of injury (61, 62). Because of their small lung volumes it is easy to unintentionally hyperventilate children during resuscitation (especially with manual ventilation) and so hypocapnea is common, which may be particularly detrimental at a time when CBF is already reduced. Abdominal injury and gastric distension easily constrain breathing because children are diaphragmatic and abdominal breathers.

SYSTEMIC ISSUES AND IMPLICATIONS FOR TREATMENT Several systemic anatomic and physiologic differences are relevant when managing head trauma in children. Young children

Figure 3 | Subdural hematomas in children. (A) Head computed tomography (CT) scan showing a typical acute subdural hematoma with a hypodensity in the ipsilateral posterior cerebral artery territory; (B) interhemispheric subdural hematoma (arrowed) with adjacent venous hypodensity; (C) subtle subdural hematoma situated on the tentorium beneath the temporal lobe; (D) minor knocks to the head can easily cause a subdural hematoma (arrowed) in children with ventriculoperitoneal shunts, especially if there is a degree of overdrainage from the shunt (13) (modified).

Figure 2 | Epidural hematomas occur in a variety of locations. (A) Head computed tomography (CT) showing a typical convexity epidural hematoma in a child; (B) evacuated hematoma in the same patient; (C) posterior fossa epidural hematoma (arrowed) underlying a suboccipital fracture; (D) epidural hematoma anterior to the left temporal tip (arrowed) (13) (modified).


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Insensible fluid losses and heat loss is common, and so hypothermia easily occurs, especially in the very young: neonates and infants have body surfaces as much as three times that of an adult, with proportionally large heads for their body size. Bones break or are deformed easily and so polytrauma is common—long bone fractures, chest wall injuries, and injuries to underlying intrathoracic and intra-abdominal organs. Rapid low dose whole body radiographs may reduce the overall radiation burden in children who have suspected polytrauma and are a useful rapid screening tool (63). Injury to solid organs is relatively common because children have proportionally larger organs (which are also closer to each other), less intraperitoneal fat and weaker abdominal musculature as protection (62, 64, 65). Focused abdominal ultrasound has a high specificity for detecting hemoperitoneum (66). Fortunately, most abdominal injuries in children can be treated conservatively (62, 67). Blood pressure control is pivotal both in the intensive care unit and in the operating room. During surgery, anesthesiologists often maintain relatively low BPs to reduce blood loss. However, this may compromise perfusion, both in handled tissues and a swollen brain. Given the importance of BP control in surgery, there is surprising variability in how hypotension is defined. For some, it is a decrease of more than 20–30% from the baseline systolic blood pressure (SBP), others use variable normograms (68). For neurosurgical patients though, we need to maintain perfusion not only of physiologically normal tissue but also of tissues penumbral to a lesion. Hypotension tolerable in normal children may cause harm in children with TBI. At the same time, high BPs cause unnecessary bleeding, as well as brain swelling if autoregulation is impaired. Hypotension must be avoided in TBI—there is a similar association between hypotension and poor outcomes in childhood TBI as in adult TBI (69). But there are several additional challenges: as stated above, BP normograms are often not used, and the circulating blood volume changes dramatically with age (70, 71). In young children, this is a small volume—“minor” blood losses can have major clinical implications. Neonates have a circulating blood volume of approximately 85–90 ml/kg, infants 75–80 ml/kg, older children 70–75 ml/kg, and adults 65–70 ml/ kg. Therefore, loss of 50 ml in a 3 kg child represents almost 20% of their circulating blood volume. The issue of BP maintenance is discussed further below.

misinterpret the likelihood of raised ICP because of these differences. The CSF-brain ratio reflects the balance between brain tissue and CSF in the ventricles and subarachnoid cisterns of the brain. Although this has not been formally quantified across the age range, radiologists and pediatric specialists are aware of the differences between very young children, older children, and adults with respect to the amount of intracranial CSF that is expected, reflecting the growth of the brain from the neonatal stage through childhood and the development of atrophy with age in adults (72, 73). As in adults, the patency of basal cisterns is an important indicator of ICP (Figure 4), but it is by no means absolute (74). Just because the cisterns are open does not guarantee that ICP is normal. Also, brain swelling can change rapidly over time, especially in children, in whom cerebral blood volume changes are a common cause of increased ICP. Therefore, what the scan looks like at one point in time may bear little semblance to what it looks like several hours later.

Cerebral Blood Flow

Understanding CBF is more challenging in pediatric TBI, in part because hyperemia is reported to be a frequent cause of raised ICP (75) and because normal CBF varies with age. These changes with age are probably the reason that diagnosing hyperemia in children is not as straightforward as it would seem (76–78), so it would be easy to misinterpret what may well be normal for a particular age group. It is also difficult to study; the data we have currently heavily depend on the tools used to determine CBF. These have included ultrasound-based techniques, MRI, and positron emission tomography (PET). The conditions under which the study is performed also markedly affect the outcome. Studies are difficult in children and so sedation or anesthesia is often used, both of which of course affect CBF. To illustrate, across three studies in children, using different techniques, the following results are reported for average total CBF: 760/781 ml/ min (girls/boys, respectively), 1,101 ml/min (girls and boys), and 1,538 ml/min (girls and boys) (79–81). Still, there are a few things we know. Rapid changes in metabolic demand in the early years follow cortical development,

BRAIN PHYSIOLOGY AND MONITORING Cerebral Compliance

Open fontanels and unfused sutures allow for increased cerebral compliance in young children, but only to a point. When intracranial volume increases rapidly, as in trauma, raised ICP is as important an issue in young children as it is in older children and adults, perhaps even more so because of the low normal range of ICP in this age group. Still, ICP monitoring is used infrequently in these children (36). Cerebral compliance is also affected by CBF and volume, and the ratio of cerebrospinal fluid (CSF) volume to brain, all of which are age-dependent. Given the differences in CSF-brain ratios, clinicians must be familiar with typical imaging across the age ranges—it is easy to Frontiers in Neurology | www.frontiersin.org

Figure 4 | Axial head computed tomography (CT) scans showing (A) relatively normal looking hemispheres with open basal cisterns (arrowed, “smiling brain”) and (B) diffuse severe swelling and obliterations of the cisternal spaces (arrowed) (74) (modified).

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progressive myelination, and synaptogenesis. CBF is lowest at birth and in neonates, peaks at ages 3–7, and then progressively decreases to adult levels (78, 80–83). CBF volume shows similar changes. The sharpest increase is in the first 6 months of life; this continues over the next 3 years at a slower pace. In 3-year olds, the CBF volume is ten times greater than in the newborn (84). CBF volume in neonates is 70 ml/min and about 700 ml/min in 3-year-old children (80). In a PET study of children, regional CBF was 140–175% of adult values for children between the ages of 3–7 years, although cerebral metabolic rates of oxygen were less markedly different (100–120% of adult values) (83). When normalized for brain volume, which of course changes with age, global cerebral perfusion (total CBF divided by brain volume) reaches a peak of around 2.5 times that of adults between the ages 3 and 4 (81, 85). But it is not just the baseline differences that matter. Pediatric brain metabolism also responds differently to activation. One study of 8–12-year-old children showed a similar percentage increase in CBF after activation but a greater increase in absolute flow when compared with adults (86). This may account for some of the dynamic changes in ICP in children with TBI despite minimal stimulus. Cardiovascular changes with age must also be considered. A higher metabolic rate in children is associated with higher cerebral and cardiac indices. A greater proportion of the cardiac output goes to the brain in children, in keeping with the higher cerebral metabolic rate—the fraction of cardiac output to the brain is more than twice that of adults (81). All of these factors affect the hemodynamic changes in ICP and CPP in children with TBI. So, when determining what CBF is in normal and pathological states, whether ischemic or hyperemic, it is clear that several age-related phenomena must be considered. Unfortunately, the evidence base is lacking because children are inherently more

difficult to study than adults, and there are few bedside tools that can be applied to children with TBI that provide good data. Transcranial Doppler (TCD) is an example of such a tool. It is commonly used but has significant limitations, in particular because only flow velocity in the basal vessels is determined. High flow velocity must be distinguished from what is normal in children based on age and what may be vasospasm. Little is written about posttraumatic vasospasm in children and unfortunately the Lindegaard ratio is not always reported, an important factor to consider when interpreting high cerebral blood velocities values by TCD (87, 88). This is the ratio between the flow velocity in the middle cerebral artery over the flow velocity in the internal carotid artery. In adult patients, it is reported that to diagnose vasospasm the flow velocity in the middle cerebral artery should be greater than 120 cm/s, and the ratio should be greater than 3 to diagnose vasospasm. To date though, this has not been validated in children. In general though, vasospasm appears to be less common in severe pediatric TBI than in adults (89); however, one study reported vasospasm in as much as one third of children (90). These figures are based on TCD parameters developed in adult subarachnoid hemorrhage patients and so may not apply to children. Much work needs to be done using bedside tools to guide hemodynamic and metabolic changes by the bedside.

Intracranial Pressure

Although it is clear that ICP is injurious to the brain as a secondary mechanism, causing brain shift and brain ischemia, with often an inverse relationship with perfusion of the brain (Figure 5), there is ongoing controversy about ICP thresholds for treatment in adult patients, recently aggravated by the South American trial of ICP monitoring in severe TBI. Although the trial has been criticized and it is currently recommended that

Figure 5 | A 15 min recording showing the influence of increased ICP and ICP reduction on brain oxygenation and brain perfusion (92) (modified). ICP, intracranial pressure (red, in mmHg); PbtO2, brain tissue oxygen (green, Licox, in mmHg); CBF, local cerebral blood flow (blue, Hemedex local tissue monitoring, in ml/100 g/min).


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existing protocols for ICP monitoring should not be changed (91), there is no doubt that greater uncertainty has crept into the management of raised ICP in trauma. Arguably, this trial may have been unsuccessful because there was a singular focus on ICP, with little consideration given to the complexity of cerebral dynamics. There are several different causes of increased ICP but recommended treatment protocols are insensitive to these. Therefore, ICP treatments may well be inappropriately applied. Furthermore, given the heterogeneity of causes of increased ICP as well as inter-individual differences, ICP thresholds for injury likely vary across patients. Lastly, all ICP therapies have adverse consequences and so the risk-benefit ratio should ideally be determined for each situation. These are some of the obvious controversies and uncertainties in managing ICP in adult TBI. To this is brought further unknowns for pediatric TBI. Much of the pediatric recommendations for TBI care are extrapolated from adult studies; there is very little pediatric-specific evidence. This is why the recommended ICP treatment threshold is also 20 mmHg (93), despite general awareness that normal ICP is lower in children and the fact that raised ICP in children behaves differently. To date, there are no age- or cause-specific recommendations for thresholds or therapies. A key starting point is knowledge of normative ICP values in children, for which there are surprisingly little data. Much of the existing knowledge derives from examination of CSF opening pressures from lumbar punctures. A series of these studies from one institution (94–97) sought to determine ICP thresholds in children. They examined children aged 1–18 years old who apparently had no condition that would increase ICP: 1,066 children were screened, the authors enrolled 472, and after exclusions investigated 197. Their results suggested that the upper limit of normal ICP for children was 28 cm H2O (20.6 mmHg). The opening pressures were normally distributed and showed a mean of 19.6 cm H2O, with 10th and 90th centiles of 11.5 cm H2O and 28 cm H2O, respectively. The authors then went on to study children who had fundoscopic evidence of optic nerve head edema and reported their results in keeping with their previous findings. Cerebrospinal fluid opening pressures are commonly used as a measure of ICP, ever since it was first described in 1891 by Quincke (98). Still, there is no general agreement that it accurately reflects ICP, especially in diseased states. Cartwright et al. studied 12 children (mean age 8.5 years) who were being monitored with an intracranial device (Camino, Integra Neurosciences) and who underwent lumbar puncture. The values were quite discrepant (p